Rapid eye movement (REM) sleep is a stage of sleep constituted by the concurrent appearance of many physiological processes and comprises about 20% of total sleep in adult humans. Despite research efforts for over 50 years utilizing modern neuroscience techniques, the biological functions or brain mechanisms subserving initiation and maintenance of this unique state of arousal are incompletely understood. The proposed project addresses the neural mechanisms that control and modulate the expression of REM sleep. Evidence supports REM sleep to be dependent on a set of anatomically distributed neural mechanisms. The sublaterodorsal nucleus (SLD), in the brainstem, is a REM sleep induction zone where the local application of GABAA receptor antagonists can result in the rapid onset of REM sleep. This implicates GABA, in interaction with mechanisms in SLD, to be involved in a negative-control of natural REM sleep. Several recent theories of REM sleep physiology put GABAergic action in SLD as central to the mechanisms controlling REM sleep expression. Yet, there are certain gaps in our knowledge that need to be filled to either support or refute these novel concepts. The objective of the current proposal is to test hypotheses relating to the nature of the GABAergic input to SLD from its two major sources, the caudal nucleus pontis oralis (PnOc) and, what we will call, the lateral pontine tegmentum (LPT). Anatomical and functional- anatomical histochemical methods, as well as behavioral pharmacology, in rat, will address the following questions: 1. Do the GABAergic neurons projecting to SLD have a REM sleep-related pattern of activation; 2. How is the GABAergic innervation of SLD organized and what receptor subtypes mediate action on REM sleep; and 3. What types of neurons in SLD receive the GABAergic input. Answers to these questions will permit a basic evaluation of the role of GABA in SLD in control of REM sleep and yield a better understanding of the mechanisms mediating sleep-state control at the cellular level. Information concerning these control mechanisms are essential to understanding the physiological process manifested during both normal and pathological sleep/wake states.